Disease relevance of PEE1

• Association between pre-eclampsia (PEE1) and the dimethylarginine dimethylaminohydrolase (DDAH) 1 and 2 genes, which play a role in the regulation of nitric oxide synthesis and release, was studied [1].
• In this report, we describe an unusual patient who, 31 years after experiencing an atypical preeclampsia-eclampsia presentation known today as the HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets), developed CAPS, which seemed to complicate a diagnosis of primary antiphospholipid syndrome [2].
• CONCLUSION: Brain edema at MR imaging in patients with preeclampsia-eclampsia was associated with abnormalities in endothelial damage markers and not with hypertension level [3].
• Preeclampsia-eclampsia: clinical and neuroradiographic correlates and insights into the pathogenesis of hypertensive encephalopathy [3].
• MATERIALS AND METHODS: Twenty-eight patients with preeclampsia-eclampsia and neurologic symptoms underwent magnetic resonance (MR) imaging [3].

High impact information on PEE1

• During high-dose insulin infusions (400 mU/m2 per min) the measured increase in energy expenditure (MEE), 150 +/- 6 cal/min, was greater than the predicted increase in energy expenditure (PEE), 72 +/- 2 cal/min, for glucose storage as glycogen [4].
• This clinical conference summarizes current concepts regarding the hypertensive disorders of gestation, focusing on the most dangerous cause, preeclampsia-eclampsia [5].
• Action of magnesium sulfate in the treatment of preeclampsia-eclampsia [6].
• Of these women, 9 had significantly elevated 17-hydroxypregnenolone (17 Preg) to 17-hydroxyprogesterone (17 Prog) ratios when compared to controls under basal conditions [7].
• Eight women had elevated ratios of dehydroepiandrosterone sulfate to androstenedione, 4 had elevations of androstenediol (Adiol) to testosterone (T), and 4 had abnormal 17 Preg to cortisol ratios [7].

Chemical compound and disease context of PEE1

• These results support the hypothesis that preeclampsia-eclampsia deplete natural lipid antioxidants and suggest that the reduced levels of vitamin A in such women experiencing hypertension of pregnancy, if they happen to be infected with the HIV-1 virus, may place them at increased risk for mother-child transmission of the virus [8].
• There were significant correlations between maternal values of total thyroxine (TT4), total triiodothyronine (TT3), thyroxine-binding globulin, free thyroxine index and birth weight of newborns in the patients with preeclampsia-eclampsia, but there was no correlation in the controls [9].

Biological context of PEE1

• Fine mapping and SNP analysis of positional candidates at the preeclampsia susceptibility locus (PREG1) on chromosome 2 [10].
• Postpartum plasma exchange for atypical preeclampsia-eclampsia as HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome [11].
• The syndrome of hemolysis, elevated liver enzymes, and low platelet count (HELLP) was first described by Weinstein in 1982 and is generally thought to represent a variant of the preeclampsia-eclampsia syndrome [12].
• Mean luteal phase serum oestradiol levels were also higher (P < 0.05) in the Prog + (1118 +/- 112 pmol/l) and Preg (2267 +/- 757 pmol/l) groups than in the Prog - (574 +/- 70 pmol/l) and control (468 +/- 38 pmol/l) groups [13].
• A review of the literature suggests that the mean arterial pressure observed during the second trimester has poor predictive value for future development of preeclampsia-eclampsia [14].

Anatomical context of PEE1

• A severity-dependent decrease was present in the nuclei of placentas with preeclampsia-eclampsia [15].
• Correlation between maternal thyroid function tests and endothelin in preeclampsia-eclampsia [16].
• Preeclampsia-eclampsia is a major cause of morbidity and mortality in mothers, fetuses, and neonates worldwide, most devastating in developing nations [17].
• The postpartum use of plasma exchange with fresh-frozen plasma was assessed in a group of seven women with severe preeclampsia-eclampsia and HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count) that persisted greater than 72 hours after delivery [18].
• These forms have been observed in contact smears prepared from 3 ml samples of peripheral circulating blood from both groups of patients, from trophoblastic tumor tissue, from contact smears prepared from placentas of patients with preeclampsia-eclampsia, and from umbilical cord blood of infants delivered of patients with preeclampsia-eclampsia [19].

Associations of PEE1 with chemical compounds

• The DHEA and PREG fractions were determined by gas chromatography-mass spectrometry, and the concentrations were converted into those of DHEA-S and PREG-S [20].
• Progesterone selectively inhibited alpha(2) GlyRs, while PREG and its acetic ester potentiated alpha(1) GlyRs [21].
• In response to ACTH, OO women had smaller responses to Adione (p less than 0.05), DHEA (p less than 0.005), DHEA-S (p less than 0.01), 17-OH progesterone (17 Prog) (p less than 0.01), and 17-OH pregnenolone (17 Preg) (p less than 0.1) [22].
• Inhibition of the aggressive behavior of castrated male mice toward lactating female intruders by dehydroepiandrosterone (DHEA) is correlated with a decrease of pregnenolone sulfate (PREG S) concentrations in brain [23].
• CONCLUSION: The study delineates an impaired catabolism of placental serotonin in preeclampsia-eclampsia [15].

Regulatory relationships of PEE1

• Correlated plasma elastase and sera cytotoxicity in eclampsia. A possible role of endothelin-1 induced neutrophil activation in preeclampsia-eclampsia [24].

Other interactions of PEE1

• Increased plasma levels of Urotensin-II in preeclampsia-eclampsia: a new mediator in pathogenesis [25]?
• The classic triad of hemorrhage (n = 8), infection (n = 5), and preeclampsia-eclampsia (n = 3) remains an important contributor (16 of 62 or 25.8%) [26].
• Among PRS cases, postpartum cerebral venous thrombosis and preeclampsia-eclampsia were the major causes of CI and CH, respectively [27].
• This review began with the clinical and pathophysiologic aspects of preeclampsia-eclampsia (Part 1) [28].
• Preeclampsia-eclampsia or normal pregnancy did not cause elevation of plasma MDA levels and GSHPx, SOD in erythrocyte [29].

Analytical, diagnostic and therapeutic context of PEE1

• The CSF content of PREG and PROG remained unaltered after treatment and failed to correlate with the SSRI-induced increase of CSF ALLO [30].
• Severe preeclampsia-eclampsia in young primigravid women: subsequent pregnancy outcome and remote prognosis [31].
• Do gravid women with preeclampsia-eclampsia ever require plasmapheresis [32]?
• The purpose of this review is to examine the pathophysiology of commonly encountered hypertensive crises, including stroke, hypertensive encephalopathy, aortic dissection, acute pulmonary edema, and preeclampsia-eclampsia and to provide a rational approach to their treatment based upon relevant pathophysiologic and pharmacologic principles [33].
• STUDY DESIGN: A retrospective cohort study was conducted on the basis of 16,936 births from January 1, 1989, through December 31, 1990, by means of data from a population-based perinatal database in Suzhou, China. Pregnancy-induced hypertension was classified as gestational hypertension, preeclampsia, or severe preeclampsia-eclampsia [34].

References